Viral hepatitis is a systemic infection predominantly affecting the liver causing damage to the liver parenchyma. Viral hepatitis cases are almost caused by one of these five viral agents: hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV). All of them are RNA viruses, except for hepatitis B, which is a DNA virus but it’s replicating like a retrovirus. Despite that they all produce clinically similar illnesses but each agent of them can be distinguished by their molecular and antigenic properties. They have a wide range of manifestation from asymptomatic to fatal acute infections, and from subclinical persistent infections to rapidly progressive chronic liver disease with cirrhosis and even hepatocellular carcinoma, common to the bloodborne types (HBV, HCV, and HDV)1.
According to WHO Global Hepatitis Report 2017, viral hepatitis caused 1.34 million deaths only in 2015. Most viral hepatitis deaths in 2015 were due to chronic liver disease (mostly cirrhosis) and primary liver cancer (mostly hepatocellular carcinoma). Internationally, in 2015, an estimation of 257 million people were living with chronic HBV infection, and 71 million people with chronic HCV infection2.
In acute hepatitis, most changes are similar whatever the cause. Hepatocytes show degenerative changes, undergo necrosis and are rapidly removed. While in chronic hepatitis, chronic inflammatory cells infiltrates comprising lymphocytes, plasma cells and sometimes lymphoid follicles are usually present in the portal tracts.
Most viral hepatitis are subclinical. But can manifest as :
– Flu-like prodrome may precede jaundice by 1-2 weeks.
– Nausea/vomiting, anorexia, headaches, fatigue, myalgia, low-grade fever, arthralgia, and urticaria (especially in HBV).
– Hepatomegaly and right upper quadrant pain.
– Splenomegaly and in some cases cervical lymphadenopathy (10-20%).